Breakthrough in Alzheimer's: Scientists managed to restore two hours of sleep without clearing the b
Recently, there have been a number of recent developments in the field of international medical health that continue to attract the attention of the industry and the public. Imagine a small fire in a corner of your kitchen. Depending on the appropriate fire extinguisher, you may be able to quickly stop it.
On the contrary, when the irrigation system is started, the entire house is flooded, turning a limited problem into a widespread disruptive problem. Researchers say that a similar situation may occur in the brains of Alzheimer's patients. Microneurons, the inhabiting immune cells of the brain, are like watermills.
Their response is designed to protect the brain, but may ultimately make it worse. A team of researchers at the University of Kent in the United Kingdom has for the first time identified this harmful process that disrupts the brain's sleep process and demonstrated how to turn it off. Dr.
McColley, Ph. D. , associate professor of physiology at Cornwall Medical School, UK, and the first author, Dr.
Nicholas Joseph Constantino, Ph. D. , the youngest PhD graduate in the UK, found that in an Alzheimer's disease animal model, microbes were the main driver of sleep loss.
When researchers used drugs to temporarily eliminate most of these cells, these animals slept for more than two hours a day. The results pointed to a potential new therapeutic focus, which Macauley called the cytoplasmic conversion syndrome. Scientists previously attributed sleep deprivation associated with Alzheimer's disease primarily to the presence of damaged neurons or amyloid plaques.
New findings suggest that this damage may have been caused by a broader immune response, similar to a whole-house reaction. Macauley says: 'Basically, we showed that not plaques themselves, nor just functional neurons, but microbes, which cause sleep disorders, but actually microglia'. Researchers studied two groups of mice that tracked sleep and brain activity to separate changes associated with Alzheimer's disease from normal changes that lead to normal aging.
One group of genes tended to produce protein patches, while the other group consisted of 'wild' mice that aged normally. The animals were examined at six months of age, when protein patches began to appear, and at ten months of age, when they represented advanced disease stages. The team used several advanced tools to closely monitor changes in sleep and brain activity.
These mice wear small earrings to more accurately monitor changes in sleep and brain activity. It should be noted that the above information is based on the results of international public research, for reference in the HealthCop, and does not constitute a clinical recommendation. If you have any health questions, please consult a professional medical professional.
